USMLE Step 1 Derm
Acne
Inflammatory disease of the skin involving the sebaceous glands and hair follicles
Pathophys
-Hyperkeratinization d/t abnormal Epithelial growth
-Androgen-stimulated hyperplasia of Sebaceous Glands
Tretinoin
MOA
-↓↓ Cohesion between Epidermal cells
-↑↑ Epidermal Cell turnover
Tx
-Acne
Lipoma
Dx
-Mature fat cells with no pleomorphism
Liposarcoma
Dx
-Lipoblasts with multiple mitoses + cause "scalloping" of the nuclear membrane
Acne
Pathophys
-Proliferation of Lipid-utilizing Bacteria within Pilosebaceous glands
Acne
Pathophys
-Excess production of Sebum
-Follicular Epidermal Hyperprolfieration
,Ecthyma Gangrenosum
Etiology
-Pseudomonas Aeruginosa
Risk Factors
-Immunocompromised
-Pts receiving Chemotherapy
Sx
-Skin patches w/ necrotic centers
-Skin ulcerations
-Hypotension
-Fevers + chills
**Although this may look like a Septic shock at first, look out for necrotic ulcers + cutaneous
lesions + immunocompromised**
Erythema Nodosum
Inflammation of Subcutaneous Fat
Risk Factors
-Sarcoidosis
Sx
-Painful erythematous nodules in the lower extremities
Histo
-Giant Cell infiltration
-Septal fibrosis
Leukocytoclastic Vasculitis
Risk Factors
-Penicillins
-Hep B
,-Hep C
-Cephalosporins
-Sulfonamides
Sx
-Non-blanching palpable purpura in bilateral lower extremities
Histo
-Markedly inflamed blood vessels
-Fibrinoid necrosis
Nevus
Benign neoplasms → "Birthmarks"
Histo
-Nests of round, uniform melanocytes that are mitotically quiescent
Allergic Contact Dermatitis
Type 4 HS
Risk Factors
-Hair Products
-Dyed Hair recently
Pathogen
-CD8+ T-cells + IFN-γ
**Pt must have had a similar rash previously in the past/Sensitization which was mediated by
Langerhans cells**
Wound Healing
In the days after initial injury, Neutrophils are recruited to the wound site and produce an
inflammatory response which helps prevent Bacterial overgrowth. However, this inflammation
also impairs formation of granulation tissue that is needed for normal wound healing. But as
the Healing process progresses, GFs and Anti-Inflamamtory CKs (I.e. IL-10) are released to
suppress the inflammatory response + facilitate Fibroblast proliferation
, **Elevated Blood Glucose stimulates the release of Pro-Inflammatory CKs**
Bullous Impetigo
Risk Factors
-Staph Aureus infection
Pathogen
-Exfoliative Toxin A (Serine Protease) which targets Desmoglein 1
Sx
-Blistering skin rash w/ Honey-colored crusts
-Vesicles + Flaccid Bullae which rupture easily
Langerhans Cells
APCs of the Epidermis which interact closely w/ T-cells
Histo
-Stellar Cells/"Racquet-shaped cells" that contain intracytoplasmic granules
Stewart-Treves Syndrome
Risk Factors
-Radical Mastectomy
Pathogen
-Chronic Lymphedema after LN dissection
Sx
-Angiosarcoma
-Firm violaceous skin nodules
Hidradenitis Suppurativa
Etiology
-Occlusion of Folliculosebaceous units
Risk Factors
-Smoking
Acne
Inflammatory disease of the skin involving the sebaceous glands and hair follicles
Pathophys
-Hyperkeratinization d/t abnormal Epithelial growth
-Androgen-stimulated hyperplasia of Sebaceous Glands
Tretinoin
MOA
-↓↓ Cohesion between Epidermal cells
-↑↑ Epidermal Cell turnover
Tx
-Acne
Lipoma
Dx
-Mature fat cells with no pleomorphism
Liposarcoma
Dx
-Lipoblasts with multiple mitoses + cause "scalloping" of the nuclear membrane
Acne
Pathophys
-Proliferation of Lipid-utilizing Bacteria within Pilosebaceous glands
Acne
Pathophys
-Excess production of Sebum
-Follicular Epidermal Hyperprolfieration
,Ecthyma Gangrenosum
Etiology
-Pseudomonas Aeruginosa
Risk Factors
-Immunocompromised
-Pts receiving Chemotherapy
Sx
-Skin patches w/ necrotic centers
-Skin ulcerations
-Hypotension
-Fevers + chills
**Although this may look like a Septic shock at first, look out for necrotic ulcers + cutaneous
lesions + immunocompromised**
Erythema Nodosum
Inflammation of Subcutaneous Fat
Risk Factors
-Sarcoidosis
Sx
-Painful erythematous nodules in the lower extremities
Histo
-Giant Cell infiltration
-Septal fibrosis
Leukocytoclastic Vasculitis
Risk Factors
-Penicillins
-Hep B
,-Hep C
-Cephalosporins
-Sulfonamides
Sx
-Non-blanching palpable purpura in bilateral lower extremities
Histo
-Markedly inflamed blood vessels
-Fibrinoid necrosis
Nevus
Benign neoplasms → "Birthmarks"
Histo
-Nests of round, uniform melanocytes that are mitotically quiescent
Allergic Contact Dermatitis
Type 4 HS
Risk Factors
-Hair Products
-Dyed Hair recently
Pathogen
-CD8+ T-cells + IFN-γ
**Pt must have had a similar rash previously in the past/Sensitization which was mediated by
Langerhans cells**
Wound Healing
In the days after initial injury, Neutrophils are recruited to the wound site and produce an
inflammatory response which helps prevent Bacterial overgrowth. However, this inflammation
also impairs formation of granulation tissue that is needed for normal wound healing. But as
the Healing process progresses, GFs and Anti-Inflamamtory CKs (I.e. IL-10) are released to
suppress the inflammatory response + facilitate Fibroblast proliferation
, **Elevated Blood Glucose stimulates the release of Pro-Inflammatory CKs**
Bullous Impetigo
Risk Factors
-Staph Aureus infection
Pathogen
-Exfoliative Toxin A (Serine Protease) which targets Desmoglein 1
Sx
-Blistering skin rash w/ Honey-colored crusts
-Vesicles + Flaccid Bullae which rupture easily
Langerhans Cells
APCs of the Epidermis which interact closely w/ T-cells
Histo
-Stellar Cells/"Racquet-shaped cells" that contain intracytoplasmic granules
Stewart-Treves Syndrome
Risk Factors
-Radical Mastectomy
Pathogen
-Chronic Lymphedema after LN dissection
Sx
-Angiosarcoma
-Firm violaceous skin nodules
Hidradenitis Suppurativa
Etiology
-Occlusion of Folliculosebaceous units
Risk Factors
-Smoking
